Receptor tyrosine kinase (RTK) co-expression facilitates tumor resistance due to redundancies in the PI3K-AKT and KRAS-ERK signaling pathways, among others. Crosstalk between the oncogenic RTKs hepatocyte growth factor receptor (MET), epidermal growth factor receptor (EGFR), and human epidermal growth factor receptor 2 (HER2) are involved in tumor resistance to RTK-targeted therapies.